Special Issue "Non-Small Cell Lung Cancer Therapies"

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (28 February 2015)

Special Issue Editor

Guest Editor
Prof. Dr. Siow Ming Lee

Department of Oncology, University College Hospital, 250 Euston Road, London NW1 2PG, UK
Website | E-Mail
Phone: +44-020 3447 9091
Fax: +44-020 3447 9055
Interests: lung cancer; HIV-related cancers; lymphoma

Special Issue Information

Dear Colleagues,

The field of non-small cell lung cancer (NSCLC) has made significant advances over the last decade. This ranges from staging classification, pathological classification, early lung screening, cytotoxic chemotherapy and new targeted treatments that have transformed lung cancer treatment for metastatic disease with molecular biomarkers. We are now entering into the new exciting era of an immunotherapy approach using drugs that can prevent NSCLC cells from evading the immune system. The purpose of this special issue is to summarize and update fellow researches as to the remarkable progress we have made for NSCLC therapies in the last several years. Both review papers and research papers are welcome.

Prof. Dr. Siow Ming Lee
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (5 papers)

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Review

Open AccessReview The Evolution of Therapies in Non-Small Cell Lung Cancer
Cancers 2015, 7(3), 1815-1846; https://doi.org/10.3390/cancers7030864
Received: 6 July 2015 / Revised: 3 September 2015 / Accepted: 7 September 2015 / Published: 9 September 2015
Cited by 55 | PDF Full-text (709 KB) | HTML Full-text | XML Full-text
Abstract
The landscape of advanced non-small lung cancer (NSCLC) therapies has rapidly been evolving beyond chemotherapy over the last few years. The discovery of oncogenic driver mutations has led to new ways in classifying NSCLC as well as offered novel therapeutic targets for anticancer [...] Read more.
The landscape of advanced non-small lung cancer (NSCLC) therapies has rapidly been evolving beyond chemotherapy over the last few years. The discovery of oncogenic driver mutations has led to new ways in classifying NSCLC as well as offered novel therapeutic targets for anticancer therapy. Targets such as epidermal growth factor receptor (EGFR) mutations and anaplastic lymphoma kinase (ALK) gene rearrangements have successfully been targeted with appropriate tyrosine kinase inhibitors (TKIs). Other driver mutations such as ROS, MET, RET, BRAF have also been investigated with targeted agents with some success in the early phase clinical setting. Novel strategies in the field of immune-oncology have also led to the development of inhibitors of cytotoxic T lymphocyte antigen-4 (CTLA-4) and programmed death-1 receptor (PD-1), which are important pathways in allowing cancer cells to escape detection by the immune system. These inhibitors have been successfully tried in NSCLC and also now bring the exciting possibility of long term responses in advanced NSCLC. In this review recent data on novel targets and therapeutic strategies and their future prospects are discussed. Full article
(This article belongs to the Special Issue Non-Small Cell Lung Cancer Therapies)
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Open AccessReview Complications from Stereotactic Body Radiotherapy for Lung Cancer
Cancers 2015, 7(2), 981-1004; https://doi.org/10.3390/cancers7020820
Received: 28 February 2015 / Accepted: 8 June 2015 / Published: 15 June 2015
Cited by 29 | PDF Full-text (600 KB) | HTML Full-text | XML Full-text
Abstract
Stereotactic body radiotherapy (SBRT) has become a standard treatment option for early stage, node negative non-small cell lung cancer (NSCLC) in patients who are either medically inoperable or refuse surgical resection. SBRT has high local control rates and a favorable toxicity profile relative [...] Read more.
Stereotactic body radiotherapy (SBRT) has become a standard treatment option for early stage, node negative non-small cell lung cancer (NSCLC) in patients who are either medically inoperable or refuse surgical resection. SBRT has high local control rates and a favorable toxicity profile relative to other surgical and non-surgical approaches. Given the excellent tumor control rates and increasing utilization of SBRT, recent efforts have focused on limiting toxicity while expanding treatment to increasingly complex patients. We review toxicities from SBRT for lung cancer, including central airway, esophageal, vascular (e.g., aorta), lung parenchyma (e.g., radiation pneumonitis), and chest wall toxicities, as well as radiation-induced neuropathies (e.g., brachial plexus, vagus nerve and recurrent laryngeal nerve). We summarize patient-related, tumor-related, dosimetric characteristics of these toxicities, review published dose constraints, and propose strategies to reduce such complications. Full article
(This article belongs to the Special Issue Non-Small Cell Lung Cancer Therapies)
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Open AccessReview Targeted Therapies in Non-Small Cell Lung Cancer—Beyond EGFR and ALK
Cancers 2015, 7(2), 930-949; https://doi.org/10.3390/cancers7020816
Received: 27 February 2015 / Revised: 7 May 2015 / Accepted: 13 May 2015 / Published: 26 May 2015
Cited by 41 | PDF Full-text (150 KB) | HTML Full-text | XML Full-text
Abstract
Systemic therapy for non-small cell lung cancer (NSCLC) has undergone a dramatic paradigm shift over the past decade. Advances in our understanding of the underlying biology of NSCLC have revealed distinct molecular subtypes. A substantial proportion of NSCLC depends on oncogenic molecular aberrations [...] Read more.
Systemic therapy for non-small cell lung cancer (NSCLC) has undergone a dramatic paradigm shift over the past decade. Advances in our understanding of the underlying biology of NSCLC have revealed distinct molecular subtypes. A substantial proportion of NSCLC depends on oncogenic molecular aberrations (so-called “driver mutations”) for their malignant phenotype. Personalized therapy encompasses the strategy of matching these subtypes with effective targeted therapies. EGFR mutations and ALK translocation are the most effectively targeted oncogenes in NSCLC. EGFR mutations and ALK gene rearrangements are successfully being targeted with specific tyrosine kinase inhibitors. The number of molecular subgroups of NSCLC continues to grow. The scope of this review is to discuss recent data on novel molecular targets as ROS1, BRAF, KRAS, HER2, c-MET, RET, PIK3CA, FGFR1 and DDR2. Thereby the review will focus on therapeutic strategies targeting these aberrations. Moreover, the emerging challenge of acquired resistance to initially effective therapies will be discussed. Full article
(This article belongs to the Special Issue Non-Small Cell Lung Cancer Therapies)
Open AccessReview Mechanisms of Acquired Resistance to ALK Inhibitors and the Rationale for Treating ALK-positive Lung Cancer
Cancers 2015, 7(2), 763-783; https://doi.org/10.3390/cancers7020763
Received: 28 February 2015 / Revised: 14 April 2015 / Accepted: 21 April 2015 / Published: 30 April 2015
Cited by 37 | PDF Full-text (711 KB) | HTML Full-text | XML Full-text
Abstract
The discovery of an echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene led to improved clinical outcomes in patients with lung cancer after the development of the first ALK-targeting agent, crizotinib. Some second-generation ALK tyrosine kinase inhibitors (TKIs), which might be [...] Read more.
The discovery of an echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene led to improved clinical outcomes in patients with lung cancer after the development of the first ALK-targeting agent, crizotinib. Some second-generation ALK tyrosine kinase inhibitors (TKIs), which might be more potent than crizotinib or effective on crizotinib-resistant patients, have been developed. Although these ALK-TKIs show an excellent response initially, most patients eventually acquire resistance. Therefore, careful consideration of the resistance mechanisms might lead to superior therapeutic strategies. Here, we summarize the history of ALK-TKIs and their underlying resistance mechanisms in both the preclinical and clinical settings. In addition, we discuss potential future treatment strategies in ALK-TKI-naïve and -resistant patients with lung cancer harboring the EML4-ALK fusion gene. Full article
(This article belongs to the Special Issue Non-Small Cell Lung Cancer Therapies)
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Open AccessReview cMET in NSCLC: Can We Cut off the Head of the Hydra? From the Pathway to the Resistance
Cancers 2015, 7(2), 556-573; https://doi.org/10.3390/cancers7020556
Received: 5 January 2015 / Revised: 19 February 2015 / Accepted: 5 March 2015 / Published: 25 March 2015
Cited by 11 | PDF Full-text (662 KB) | HTML Full-text | XML Full-text
Abstract
In the last decade, the tyrosine kinase receptor cMET, together with its ligand hepatocyte growth factor (HGF), has become a target in non-small cell lung cancer (NSCLC). Signalization via cMET stimulates several oncological processes amongst which are cell motility, invasion and metastasis. It [...] Read more.
In the last decade, the tyrosine kinase receptor cMET, together with its ligand hepatocyte growth factor (HGF), has become a target in non-small cell lung cancer (NSCLC). Signalization via cMET stimulates several oncological processes amongst which are cell motility, invasion and metastasis. It also confers resistance against several currently used targeted therapies, e.g., epidermal growth factor receptor (EGFR) inhibitors. In this review, we will discuss the basic structure of cMET and the most important signaling pathways. We will also look into aberrations in the signaling and the effects thereof in cancer growth, with the focus on NSCLC. Finally, we will discuss the role of cMET as resistance mechanism. Full article
(This article belongs to the Special Issue Non-Small Cell Lung Cancer Therapies)
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